The hair cells and supporting elements in the avian ear can regenerate after being damaged by ototoxic drugs or acoustic overstimulation resulting in the partial, or in some cases, complete recovery of hearing. However, relatively little is known about the biological mechanisms that regulate or limit the recovery of auditory function at the level of the cochlea. The overall goal of this project is to determine what functional deficits are present in the neural output of the cochlea when the hair cells, tectorial membrane or afferent dendrites are damaged and then to determine how quickly and to what extent these neurophysiological deficits recover as these anatomical structures regenerate or are repaired. Three different agents will be used to selectively damage different cochlea structure; kanamycin selectively destroys all the hair cells; intense acoustic stimulation selectively destroys only short hair cells and associated tectorial membrane; kainic acid selectively destroys the afferent dendrites. The destruction and regeneration of these structures will be assessed by light, fluorescence and transmission electron microscopy. The functional deficits and recovery process will primarily be assessed by recording from and then labeling single cochlea ganglion neurons. The proposed experiments will answer the following questions. What functional deficits are associated with the permanent loss of short hair cells? Does the cochlear frequency-place map change when short hair cells are missing or when the short and tall hair cells regenerate? What neurophysiological deficits are present in cochlear ganglion neurons that innervate regenerated hair cells: How long does it take for the cochlear afferent dendrites to become functionally mature in the presence of intact hair cells? Do the kanamycin and kainic acid treatments reduce the number of cochlear ganglion neurons? The results of these studies will provide new insights into the mechanisms that lead to the partial or complete recovery of auditory function when the hair cells and supporting elements in the inner ear regenerate.